Nutrition & fluid balance digestive (class 6) Flashcards
factors affecting nutritional status in elderly
changes in appetite, taste, smell, and GI affect nutrition.
decrease income contributes to food intake.
dentures, missing teeth, pain from poor oral hygiene.
chronic illness/depression
multiple medications
cognitive impairment/dementia
living in LTC facility.
elderly nutrition teaching
maintain healthy weight.
chose nutrient dense foods.
oral care BID
avoid processed foods & high fat foods.
nutritional needs in elderly
metabolism slows with age less calories needed.
vitamin and mineral needs same.
iron needs drop for post-menopausal women.
vitamin D synthesis reduced.
vitamin B12 reduced.
fluids-about 8 cups/day.
limit alcohol, refined sugars, fat, and salt.
zinc deficiency can alter taste.
risk factors of dehydration in elderly
purposely restrict their fluids. loose sense of thirst. forget to drink. cannot get fluids on their own. No a/c in summer.
s/s dehydration in elderly
confusion-change in mental status early s/s dehydration.
dry tongue & mucous membranes (furrowed tongue).
skin turgor less reliable (sternum or inner thigh)
tachycardia
subnormal temperature.
pinched facial expression
hot dry body.
nursing interventions
dehydration in elderly
I&O. daily weight (3% loss sign of dehydration).
monitor electrolyte levels.
assessment for deficient fluid volume.
encourage fluids.
call light in reach.
review orders for NPO status & notify physician for late & cancelled tests.
Oral cancer
malignancy of oral mucosa on lips, tongue, floor of mouth, or oral tissues.
high morbidity & mortality.
40 years old most common.
oral cancer
risk factors
smoking, drinking alcohol, chewing tobacco, HPV-recent studies have found.
oral cancer
symptoms
early: painless ulcer or lesion.
later: difficulty speaking, swallowing, or chewing, swollen lymph nodes, blood-tinged sputum.
leukoplakia: white patch smokers patch.
erythroplakia: red vevety patch.
any oral lesion that doesn’t heal/respond to Tx in 1-2 weeks should be evaluated for malignancy.
oral cancer
treatment/prevention
eliminate causative factors (smoking, tobacco, ETOH)
oral sex & HPV transmission.
regular dental care.
stages I&II are highly curable: surgery & radiation.
stage III&IV require combination: surgery, radiation, & chemotherapy. radical neck dissection with tracheostomy.
effects of oral radiation
males may experience permanent loss of hair in area of their beard.
skin irritation and lack of salivary function-worse as treatment continues.
salivary function may not return to normal: keep mouth moist, HOB elevated, Additional fluids.
esophageal cancer
uncommon & high mortality rate.
<5% survive 5 yrs after diagnosis.
most tumors in lower 1/3 of esophagus
esophageal cancer risk factors
cigarette & chronic ETOH abuse. opiate smoking. ingested carcinogens. chronic reflux. physical mucosal damage.
esophageal cancer
symptoms
most common: progressive dysphagia & recent weight loss. anemia. GERD-like symptoms anorexia chest pain persistent cough.
esophageal cancer
goal
control dysphagia and maintain nutrition regardless of treatment
esophageal cancer
diagnosis
bronchoscopy.
barium swallow
chest xray, CT scan, MRI look for metastasis
esophageal cancer treatment
radiation therapy and or chemotherapy
esophagectomy & possible anastomosis of the stomach to remaining esophagus.
NG tube often post op plaed in OR
esophageal cancer
complications
anastomosis leak.
respiratory complications (pneumonia, acute respiratory distress syndrome)
gastric necrosis or bleeding
infection & sepsis.
stomach cancer
risk factors
H. pylori infection is majore factor 60-90%.
genetic.
chronic gastritis.
gastric polyps.
carcinogens in the diet (smoked foods & nitrates)
history of partial gastric resection.
stomach cancer
symptoms
early symptoms: very few.
vague-feeling of early satiety. anorexia, indigestion and vomiting.
ulcer-like pain unrelieved by antacids after meals.
advanced disease: weight loss.
cachectic (malnourished & poor health)
palpable abdominal mass.
occult blood in stool
stomach cancer
diagnosis
anemia may be first symptom (CBC)
upper GI with barium swallow xray
ultrasound
upper endoscopy with visulatization and biopsy of lesion=provides definitive diagnosis.
stomach cancer
treatment
removal of part of all of the stomach.
post-op nursing care for gastrectomy
assess NG tube & suction as ordered.
do not replace or move tube. call DR.
assess color amount & odor of gastric drainage. initial NG output is bright red then to green-yellow over 2-3 days. if excessive amount of bright red, call DR.
monitor bowel sounds and distention.
encourage ambulation.
monitor weight.
complications of gastrectomy
dumping syndrome common: food eaten enters small intestine too quickly, gastric surgery makes it more difficult to regulate movement.
s/s: occurs 5-30 mins after eating.
feeling full, abd cramping, nausea, vomiting, severe diarrhea, sweating, flushing, or light-headedness, rapid heartbeat, loud hyperactive bowel sounds, hyperosmolar chyme in the jejunum causes rapid rise in glucose & release of excessive insulin. hypoglycemia common 2-3 hr after meals.
dumping syndrom management
small frequent meals, liquids & solids taken at separae times not together. increase protein & fats. reduce CHOs especially simple sugars. recumbent/semi-recombent 30-60 min after meals.
monitor nutritional status.
liver functions
metabolism of proteins fats & CHO.
produces bile for fat absorption & eliminates bilirubin from body. detoxifies ETOH & other toxic substances. inactivates drugs/limits duration of effects. metabolism of steroid hormones & most drugs. makes blood proteins. ammonia is converted to urea for kidneys to excrete. minerals and fat soluble vitamin storage. stores iron as ferritin which is released as needed for RBC production.
common manifestations of liver disorders
hepatocellular failure. jaundice. portal hypertension
hepatocellular failure
liver is vital to:
digestion & metabolism of nutrients. production of plasma proteins. clotting proteins. albumin.
metabolism & excretion of bilirubin, steroid hormones, toxins, and ammonia.
note: albumin keeps fluid in the vessels. low albumin=fluid leaks out of vessels causing edema/ascites.
hepatocellular failure.
impaired function of liver cell causes
decreased production of albumin r/t impaired protein metabolism.
decreased production of clotting factors.
decreased bile production which impairs absorption of lipids & fat soluble vitamins (VIT K affects production of clotting factor.)
impaired metabolism of steroid hormones causing: feminization of men & irregular menses in women.
hepatocellular failure/jaundice
RBCs breakdwon & form bilirubin. when bilirubin cant be emulsified & digested through bile it builds up causing yellow appearance.
accumulation of bilirubin in tissues caused by disruption in metabolism of bilirubin=yellow color reflected in skin , mucus membranes, sclera.
protal hypertension
impaired blood flow through liver increases pressure venous system that drains the GI tract, spleen, & surface veins of the abdomen causing:
veins in GI tract & abdominal wall to dilate causing: appetite suppresion, formation of collateral vessels in esophagus, rectum, & stomach. esophageal varices, hemorrhoids, caput medusa.
ascites: increased pressure in abd vessels causes fluid to leak out. worse by low albumin levels.
hepatic encephalopathy build up of ammonia waste product causing mental status changes.
diagnostic studies of hepatic function
labs: ALT(alamine aminotransferase)
AST(asparate aminotransferase)
ALP(alkaline phosphatase)
bilirubin total direct (conjugated) indirect (unconjugated)
albumin: protein in plasma produced by liver.
decrease levels cause fluid shift from vessels into tissues causing edeme & ascites.
increased levels seen in dehyrdation
ammonia: a by product of protein metabolism converted by liver to urea for excretion by kidneys.
increase levels can cause confusion, behavioral & personality changes.
low protein diet.
paracentesis
aspiration of fluid from peritoneal cavity.
paracentesis NI pre procedure
void prior to decrease risk of bladder puncture. weight and abdominal girth measurements. R provides measure of effectiveness of procedure. position seated (side of bed or chair) with feet supported. sllow fluid to collect in lower abdomen facilitating removal.
paracentesis
post procedure
monitor puncture sites & vitals for s/s of hypovalemia.
may be some leaking at puncture site-normal depedning on how much fluid remains.
weight and abdominal girth @ umbilicus.
record amount color clarity of fluid removed no more than 2L removed generally.
albumin often given to retain fluid in vascular system & decrease complications.
liver biopsy
performed to:
r/o cancer, detect cysts.
detect cirrhosis.
- need driver home. NPO 4-6 hrs prior, signed consent. place on right side 1-2 hr after. bedrest 8-10hr after procedure home. light activity 1-2 wk after. ask about anticoagulants taken or NSAID use.
teach: pain in right shoulder common as local anesthetic wears off.
- need driver home. NPO 4-6 hrs prior, signed consent. place on right side 1-2 hr after. bedrest 8-10hr after procedure home. light activity 1-2 wk after. ask about anticoagulants taken or NSAID use.
prothrombin time (PT/ pro time)
measures clotting ability of fibrinogen and prothrombin. increase levesl can indicate liver disease.
normal range 10-13
common hepatotoxins
drugs: isoniazid, acetaminophen, thiazides, tetracycline, statins, steroids, alcohol, some herbal supplements.
cirrhosis
fibrosis (scar tissue) of liver tissue leading to:
decrease mass, impaired liver function, altered blood flow.
thought to be irreversible but fibrosis may be reversed when underlying cause eliminated.
types of cirrhosis
alcoholic: lannec’s
posthepatic: (hapatotoxic, viral hepatitis, nonalcoholic fatty liver r/t obesity, autoimmune hepatitis)
Biliary: obsructions.
alcoholism major cause.
multisystem effects of cirrhosis
ascites- accumulation of plasma fluid in abdominal cavity. pt in semi fowlers positiion to facilitate breathing.
bleeding-decreased clotting factor, platelt destruction, & impaired vit k absorption.
esophageal varices & hemorrhoids: increase pressure inportal system & thin walled vessels cause this.
mutlisystem effects of cirrhosis
encephalopathy: r/t build up of ammonia as liver cannot convert to urea for excretion.
integumentary: pruritis r/t build up of toxins.
malnutrition- r/t impaired fat & nutrient absorption. supplements needed.
maifestations of cirrohisis
malaise, fatigue r/t anemia, GI-gastritis, anorexia, diarrhea. malnutriton: malabsorption of vitamins. fluid retention-edema/ascites.
jaundice-liver & bile duct inflammation prevents bilirubin from being excreted into small intestine.
bleeding-bruising.
encephalopathy
pain & pruritis.
cirrhosis management
TIPS procedure( trans jugular intrahepatic portosystemic shunt)
relieves portal HTN & complications of esophageal varices & ascites.
needle inserted transcutaneous creating a channel.
expandable metal stent inserted to allow blood flow from portal vein to hepatic vein.
bypasses the cirrhotic liver.
short term treatment until liver transplant.
liver tumors
primary liver cancer uncommon. prognosis poor r/t advanced by time diagnosed.
risk factors of liver tumors
chronic hep B & C infections. cirrhosis. chronic alcohol consumptions.
non-alcoholic fatty liver.
s/s liver tumors
jaundice ascites, edema extreme weakness. GI bleeding, bleeding tendancies. high AFP alpha=fetoprotein. encephalopathy. spreads quickly painful palpable mass RUQ
liver tumor diagnostics
CT scan.
MRI
liver biopsy
liver tumor treatments
radiation, chemo, tumor excisions, liver transplant.
hepatitis
inflammation of the liver usually caused by virus. can be acute or chronic.
chronic hepatitis increases risk of liver cancer.
viral hepatitis
hep A, B, C, D, E virus.
chronic hepatitis
primary cause of liver damage leading to cirrhosis & liver cancer cuase but HBV HCV HDV.
fulminant hepatitis
rare rapid progression liver failure 2-3 wk associated with HBV and HDV
autoimmune hepatitis
body attacks itself.
pre-icteric(prodromal) phase hepatitis
begins abrupt or insidiously. malaise, fatigue, anorexia, muscle aches. often mistaken for flu.
icteric (jaundiced) hepatitis
begins 5-10 days after onset of symptoms. jaundice sclera, skin, mucous membranes. pruritus r/t bile salts on skin. stools light brown or clay r/t bile not excreted in stool. brown urine from bile pigment excreted y kidneys instead.
recovery/posticteric phase hepatitis
follows jaundice & lasts several weeks. s/s gradually improve. serum enzymes decrease.
carrier states
carrier state is when an infected person harbors active virus & is capable of spreading it to others even though there are no manifestations of the disease.
hep B & C associated with carrier states.
hep A
infectious hepatitis.
prevent: Hep A vaccine. give immunoglobulin IM within 2 wk of exposure.
transmission- fecal-oral via contaminated food, water, or direct contact with infected person.
present in stool up to 2 wks before s/s present.
risk factors & onset: internation travel, close household contact, abrupt onset, self-limiting disease.
hep B
can cause acute, chronic, rapid progressing hepatitis. associated with a carrier state.
may be asymptomatic.
preventable vaccine available. hep B immunoglobulin IM within 24 hr exposure.
transmission contact with infected blood & body fluids.
high risk: injection drug users. multiple sex partners & gay sex. exposure to frequent blood products. healthcare workers thru blood & needle stick injury.
complications: primary liver cancer-especially if infected perinatally.
hep C
** no vaccine available.
treat with interferon (antiviral)
primary cause or chronic hepatitis, cirrhosis, & liver cacner.
acute hepatitis usually asymptomatic.
transmission: infected blood & body fluids.
risk factors: injection drug use primary.
s/s chronic: fatigue, hepatomegaly, occasional jaundiced periods, liver enzymes elevated.
labs for hepatitis
ALT increase, AST inrease, ALP increase, serum bilirubin increase, viral antigen & specific antibodies-identifies virus & state of activity.
liver bipsy-detect & evaluate for chronic hepatits.
pancreas function
glanular organ that provides 2 functions (exocrine & endocrine)
produce enzymes that affect control of digestive enzymes.
produce hormones for carbohydrate, fat, and protein metabolism.
pancreatitis
inflammatory disorder involves self destruction of pancreas by its own enzymes. leads to hemorrhage & necrosis.
exact causes unknown. alcoholism & gallstones primary risk factors for acute pancreatits.
acute or chronic
diagnostic tests pancreatic function
serum amylase inrease in pancreatitis.
serum lipase increase.
endoscopic retrograde
cholangiopancreatography (ERCP) diagnostic for chronic pancreatitis to differentiate fibrosis from carcinoma.
acute pancreatitis
often mild & self limiting. reversible. abrupt onset of epigastric & LUQ pain. gallstones leading cause. ETOH 2nd cause.
interstitial edematous pancreatitis
milder leads to inflammation & edema of pancreatic tissue.
necrotizing
more sever leads to inflammation, hemorrhage, and necrosis of pancreatic tissue.
pathophysiology of acute pancreatitis
activated pancreatic enzymes released into pancreas.
enzymes, trypsin, digests pancreatic tissue & activates other enzymes.
other enzymes digest blood vessel walls causing vasoldilation leading to edema.
fluid volume shifts from circulation blood into retroperitoneal spaces of abdomen.
hypovolemic shock & renal failure can develop 24 hr after onset.
chronic pancreatitis
chronic inflammation, fibrosis, gradual destruction of pancreatic tissue.
irreversible
alcoholism primary risk factor in US.
ETOH- pancreatic secretions have insoluble proteins that calcify & block pancreatic ducts & flow of pancreatic juices
10-20% idiopathic.
recurent infammation.
acute
reversible, onset abrupt/24 hr. gallstones leading cause.
complications: intravascular volume depletion, renal failure, acute resp distress syndrom.
chronic
irreversible. onset gradual destruction
alcoholism leading cause.
complications:malabsorption & malnurtition. increase risk of pancreatic cancer. opioid addiction r/t pain.
acute manifestations
abrupt sever epigastric LUQ pain. N/V, fever, decrease bowel sounds, abd rigidity & distention. tachycardia, hypotension, cold clammy skin. possible jaundrive. turner+(flank bruisng) Cullen sign (peri-umbillical bruising)
chronic manifestations
recurrent epigastric & LUQ pain radiating to back. anorexia, nausea, vomiting, weight loss, flatulence, constipation, steatorrhea (fatty foul smelling stool)
acute treatment
supportive: pain meds. NPO, IVF to maintain vascular volumer. TPN nutrition while NPO. low fat high CHO diet when bowel sounds +, pain relieved, & amylase normalizes 3-4days. surgery if cause gallstones.
chronic treatment
pain meds-monitor dependence. enzyme supplements-manage abd pain & reduce steatorrha. high CHO low fat diet with frequent feedings. H2 blockers & ppo to neutralize gastric secretiosn
pancreatic cancer
uncommon <3% of cancers but one of most letha.
pancreatic cancer risk factors
cigarette smoking 2x higher risk, chronic pancreatitis, DM, cirrhosis, obesity, high fat diet, genetic predisposition.
pancreatic cancer manifestations
few s/s until advanced. dull epigastric pain that increases as tumor grows. wt loss, flatulence.
pancreatic cancer treatment
early may be able to resect head of pancreas (whipple)
pancreatoduodenectomy (WHipple)
radiation, chemo.
post-op whipple complications
hypovolemic shock, hemorrhage, bile leak, hepatorenal failure.
whipple procedure
done when cancer found early. removes head of pancreas, entire duodenum, distal 1/3 of stomach, portion of jejunum
whipple procedure nursing care
semi-fowlers-facilitate lung expansion, reduce stress on suture line. maintain NG low int. sx keep patent. do not reposistion puts stress on suture lines. no forceful NG irrigations-stress on suture lines.
